CNS infections 1 Flashcards

(75 cards)

1
Q

Most Common Agents of Congenital Infections

A

TOxoplasma,
Rubella,
Cytomegalovirus [CMV],
Herpes simplex virus [HSV]) -2 or -1

TORCH test: a series of tests for specific IgM in chord blood
(may be STORCH: syphilis)

one more: Lymphocytic choriomenigitis virus (LCMV)

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2
Q

HSV infections cause infection and morbidity in neonates:

areas ?

A

Skin, Eye, Mouth
CNS disease
Disseminated disease with or without CNS disease

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3
Q

the leading cause (by far) of infection and morbidity in the neonate

A

CMV
40,000 neonates born in US/yr affected–>sequelae (hearing loss, vision loss, and cognitive impairment) in 1/5th of cases

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4
Q

nosocomial-acquired meningitis orgs

*half of all meningitis cases in US

A

Gram-positive cocci:
Staphylococcus aureus
coagulase-negative staphylococci
non-pneumococcal streptococci

Gram-negative rods

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5
Q

Predisposing conditions for Nosocomial-acquired meningitis

A

recent neurological procedures.
presence of neurological devices.
altered immune status

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6
Q

??? is NOT a portal of entry for viral infection

A

the brain

Infection in the CNS is usually a secondary infection, occurring days, weeks, months, or years after the initial infection

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7
Q

bacterial meningitis vs. viral meningitis

A

less common

used to be more but now we vaccinate against mumps?

many not def. ddx
devastating sequelae

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8
Q

bac meningitis neonate orgs

A

Streptococcus agalactiae, Escherichia coli

K. pneumoniae

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9
Q

bac meningitis infant and young kiddo orgs

A

N. meningitides
S. pneumoniae
Myobacterium tuberculosis.

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10
Q

bac meningitis adolescents →Elderly orgs

A

N. meningitides
S. pneumoniae

> 50-y-o: L. monocytogenes

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11
Q

The problem for the physician is to differentiate between bacterial pyogenic/purulent meningitis, which is a ?? and ?? viral meningitis

A

medical emergency

benign

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12
Q

Symptoms of bacterial meningitis in the older child → adult include acute onset of:

A

*irritability
*lethargy (altered mental status)
*fever
severe headache
nuchal rigidity
vomiting
opisthotonos
pressure on eyeball
photophobia

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13
Q

the single most important predisposing factor for meningitis in the neonate

A

Low birth weight

Low birth weight (LBW;

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14
Q

What factors predispose the LBW, VLBW, and ELBW infant to infection?

A

Impaired innate and adaptive immune functions

if Require nosocomial techniques and devices to keep alive

Incidence of sepsis is much higher

Maternally related events allow agent access to fetus before birth or during parturition

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15
Q

Impaired innate and adaptive immune functions

A

Antibodies production and PMN (both in number, function) are poor in newborn, especially in prematurely born infants

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16
Q

nosocomial techniques and devices

A
Are often kept in 80% humidity, an environment where bacteria & fungi flourish.
Presence of multiple invasive devices:
catheters
feeding tubes
suction tubes
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17
Q

Maternally related events allow agent access to fetus before birth or during parturition, such as

A

Premature rupture of membranes, esp. for greater than 24 hours.

Maternal infection during last week of pregnancy, e.g.,
vaginosis,
UTI
cervicitis
chorioamnionitis

Excessive manipulation during delivery

Use of intrauterine monitoring devices

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18
Q

Sources of etiologic agent:(neonate meningitis)

A

Infection acquired in utero (Common source):
From infected chorioamnionic and amniotic fluid.
From infected blood – via chord blood – transplacental transmission.

Infection during parturition, aspiration of infected vaginal secretions (Common source).

Infection acquired hours → days post-partum from caregiver(s).

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19
Q

Signs and symptoms of meningitis in the neonate are not the same as the adult and include:

A

Fever
Lethargy
Poor feeding
GI disturbance (vomiting/diarrhea)/abdominal distension
Respiratory abnormalities (e.g., dyspnea, cyanosis)
Cardiac abnormalities (tachycardia)
Bulging fontanelle

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20
Q

neonatal meningitis px

A

generally poor, mortality rates vary from 10-60% with survivors showing some permanent defects (neurological sequelae) which may be significant

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21
Q

Streptococcus agalactiae - Group B Streptococci (GBS):

A

Gram-positive cocci in chains or pairs (AKA streptococci).

β-hemolytic on sheep blood agar via production of the ornithine rhamnolipid pigment or lipid toxin.

Bacitracin-resistant versus GAS, which is bacitracin- sensitive

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22
Q

S. agalactiae group based on ??

A

cell wall antigen

Lancefield’s serological classification based primarily on cell wall carbohydrate (C carbohydrate, teichoic acids). Groups A→T. Groups A, B, D are clinically important.

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23
Q

S. agalactiae also serologically typed based on ??

A

capsular polysaccharide:

Major virulence factor –

There are several (9) groups:

Five groups (especially Group III) are most common causes of both early and late onset disease.

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24
Q

S. agalactiae is the leading cause of ?? alone or with ?? within the first 3 months of life

A

bacteremia
meningitis and/or pneumonia as complications

Incidence is highest in pre-term, but most (75%) cases occur in full-term infants (more of those guys)

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25
1/3 of all invasive GBS disease occurs in ??
pregnant women (Maternal UTI caused by GBS frequently occurs before or just after birth).
26
adults, esp. elderly can also get GBS
usually with chronic or immunosuppressive disease: persons > 60 y-o-age is high (4 → 7 cases/100,000 population) with a high (25%) mortality rate. Diabetes, cirrhosis, malignancy, AIDS. *Clinical GBS syndromes occur in virtually all tissues/organs
27
GBS Transmission and Reservoir:
Vertical infection occurs before and/or during birth Horizontal infection (mother/caregiver → newborn) occurs after birth. Agent colonizes mother’s pharynx, vagina, and skin via rectal colonization: - Not all gravid females are colonized by GBS. - Not all gravid females colonized by GBS pass it to the neonate. - Not all neonates carrying GBS become infected/diseased. *no seasonality
28
Two forms of neonatal disease are recognized:
Early (acute) onset sepsis (bacteremia) Late (insidious) onset sepsis (bacteremia or focal infection)
29
Early (acute) onset sepsis (bacteremia):
Occurs within the first 6 days after birth. Source is mother, infection is acquired in utero or via passage through birth canal. More common form of disease (80% of cases)
30
Late (insidious) onset sepsis (bacteremia or focal infection):
Occurs 7 days → 3 months following birth. Source: associated with postpartum acquisition in the nursery (care givers) or community or mothers. ``` Focal infections include: meningitis cellulitis osteomyelitis septic arthritis. ``` Less common form of this disease (20% of cases)
31
Meningitis occurs in few (5%) cases of ?? but many (@30%) cases of ??
early onset sepsis late onset sepsis Because of the higher mortality rate and the occurrence of neurological sequelae associated with meningitis, have a high index of suspicion for meningitis
32
hemolytic GBS pigment triggers mast cell degranulation, resulting in the release of ?? mast cell degranulation in the lower genital tract can limit colonization of ??
preformed and proinflammatory mediators hyperpigmented GBS strains
33
``` Isolation of GBS from: the patient (i.e., neonate) from normally sterile sites: ```
CSF blood lungs
34
Isolation of GBS from: the mom
vagina. nasopharynx. GI tract/anus. skin.
35
Identification of the organism:
Rapid slide agglutination to ID GBS, based on C-specific substance/carbohydrate. other tests - PCR
36
The screening approach for GBS:
all pregnant mothers be screened at 35→37 weeks gestation (Studies show that this is best approach) 2 specimens are collected, swabs from rectum and vagina all identified carriers and women who deliver pre-term before screening should be offered intrapartum antimicrobial prophylaxis iv
37
intrapartum antimicrobial prophylaxis iv (GBS)
Penicillin G ampicillin if penicillin-intolerant: Cefazolin Vancomycin if: susceptibility to erythromycin and clindamycin has not been performed or has been found resistant
38
GBS: antibiotic prophylaxis before labor starts and single administration of postpartum antibiotic prophylaxis for newborns are ??
ineffective
39
There are no reports of resistance to ?? but GBS resistance to ?? and ?? has been reported at 15-30% and 10-20% of cases, respectively
penicillin G | erythromycin, clindamycin
40
The risk factors assessment (non screening)approach for GBS
intrapartum antimicrobial agents (same antibiotics as stated above administered iv) should be offered to any pregnant women with 1 or more of the following risk factors: elevated intrapartum temperature membrane rupture > 18 hours premature onset of labor premature rupture of membrane (PROM) at
41
Many (NOT ALL) hospitals have adopted the CDC recommendations or give all mothers antibiotics and this has resulted in ??
a BIG decrease in GBS infections in neonates in US
42
There is no prevention strategy for ??
late onset GBS disease
43
Problems with Intrapartum Antibiotic Exposure: with increased use of intrapartum antibiotics to reduce the incidence of neonatal GBS infection, the incidence of early onset sepsis in VLBW infants has not changed, but the ??? have changed
etiologic agents responsible e.g., E. coli are now the primary etiologic agents therapy is resulting in an increased incidence of late onset sepsis
44
Listeria monocytogenes
A Gram positive, coccobacilli (rod), motile, coryneform species. (may look like cocci but are NOT) Not fastidious. Growth temperature range is broad (0→50o C). Isolated by cold enrichment, like Yersinia.
45
L. mono are IC or EC??
facultative intracellular pathogens Invade & multiply in nonprofessional phagocytes: epithelial cells. endothelial cells. Survive and multiply within phagocytic cells such a: non-activated macrophages and monocytes. enterocytes.
46
Listeria is Serologically heterogeneous
Numerous serotypes based on O & H antigens *Three serotypes account for most infections in animals and humans
47
Virulence factors of listeria
Lipoteichoic acids (LPS-rare for G+): Immunomodulator as potent Proteins: enzymes required for organism-directed phagocytosis and cell-to-cell spread.
48
Listeria incidence
sporadic cases and food-borne epidemics.
49
Listeria Transmission and reservoirs
Food-borne: ingestion is primary mode, esp. adults, rare disease but mortality is high. Human-to-human: in utero - transplacental (vertical) transfer. during parturition (vertical) transmission. Animal-to-human; a zoonosis.
50
Primary reservoirs: Listeria
distributed worldwide – is ubiquitous: soil water normal fecal flora of mammals - including humans: Human immune carriers exist. food (tons!)
51
Age and gender and seasonality of Listeria
preggos | SUMMER: food assoc.
52
Listeria risk factors
Immunosuppression - T cell suppression: These are the populations for which you should have a high index of suspicion of listeriosis!: young/neonates (3rd leading cause of invasive neonatal disease). Aged/elderly persons: >70 y-o-age (2/100,000), Pregnant females (12/100,000), Advanced HIV/AIDS pt: (70→210/100,000), Other: Immunosuppressive therapy (esp. T cell deficiencies) Cancer Diabetes
53
Incidnce of Listeria in the general population is ?? most cases due to ??
rare! Sporadic disease NOT common-source outbreaks
54
Listeria pathogenesis
Organism is ingested → passes through the intestinal epithelium → bacteremia
55
Listeria POE is the ??
GIT Agent is phagocytized by gastrointestinal cells (without damaging the integrity of the GI tract) and macrophages (agent survives in non-activated macrophages). Concurrent/Intercurrent GITI with another pathogen may promote infection with Listeria?
56
?? induce phagocytosis of Listeria by nonprofessional phagocytic cells (similar to Shigella) and also mediate entry into epithelial cell
Surface proteins
57
Enzymes (esp. ??) disrupt the phagosome membrane allowing Listeria cells to escape from the host vacuole and replicate in the host cell cytoplasm
listeriolysin O
58
Cell-to-cell infection occurs when a tail of ?? form at the ends of the Listeria cells due to virulence factors, e.g., ?? Same mechanism is used by ??
polymerized actin filaments ActA Shigella sp., Rickettsia and vaccina virus
59
Listeria has a tropism for
CNS (meninges and brain, especially the brain-stem) and is capable of penetrating and infecting brain parenchyma (usually brain stem). placenta.
60
Listeria incubation period
may be long (about 30 days; range is 11→70 days).
61
Listeria immunity
Primarily T cell-mediated immunity control of infection requires activated macrophages, which can only kill *stationary (latent*) phase Listeria* (better pathogen than Mtb!)
62
Listeria Infections in pregnancy: occurrence and manifestations
Illness usually occurs in the 3rd trimester, with the greatest decline in gravid female’s CMI. Gravid female manifests with acute, febrile illness - severe flu-like symptoms due to bacteremia. Mother rarely manifests with CNS infection
63
Outcomes of Listeria Fetal (in utero) infection: fetal mortality?
early-onset sepsis syndrome, spontaneous abortion (from 5m gestation on), stillborn, premature births. Fetal mortality rate is high (15→50%).
64
Listeria Early-onset sepsis syndrome:
is associated with prematurity. Infection is likely acquired in utero via inhalation of infected amniotic fluid. ``` Agent is found in neonate practically everywhere (in the: external ear nose throat blood CSF *lungs *gut ``` Symptoms manifest in newborn (
65
Listeria Granulomatosis infantisepticum is ?? agent found in ??
a rare condition involving in utero infection disseminated abscess and/or granulomas in multiple internal organs, esp. liver & spleen. papules in throat, skin may also be present. Neonate mortality rate is high (>50%).
66
Listeria Late-onset meningoencephalitis
Infection occurs during or after birth. Symptoms manifest in between 1→2 weeks postpartum. Neonate mortality rate is moderate (10 → 20%). Mother is asymptomatic.
67
Adults w/ Listeriosis manifest with one or more of:
Meningitis (acute or subacute) Meningoencephalitis Encephalitis Macroscopic brain abscess (mass lesions) with meningitis: Seizures can occur *Listeria has tropism for brain (esp. brain stem). Bacteremia may → flu-like disease. Predisposing factors as stated above. Food poisoning/gastroenteritis Focal non meningeal infections are uncommon
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Listeria Food poisoning/gastroenteritis symptoms include: occurs in who ??
``` fever headache arthropathy & myalgia non-bloody diarrhea abdominal cramps, nausea, vomiting ``` Occurs in both immunocompetent and immunocompromised persons
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Listeria ddx: based on
etiologic agents based on population
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Listeria dx: Cx
sedimented CSF. amniotic fluid. blood (esp if pt. spikes or has a fever). tissues including placenta. feces (if present, present in low numbers [20 CFU/g feces]) so prolonged, cold-enrichment may improve chances of isolation. detection in food (must be same serotype as that isolated from patient to prove source).
71
Listeria dx: Gram stain
``` Sources: sedimented CSF. amniotic fluid. blood (esp feces. ```
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Listeria dx: Gram stain limitations ??
morphology similar to either Corynebacterium sp. or coccobacilli. easily decolorized (appear Gram-negative or not stained). present in small numbers in feces, so easily missed
73
Listeria dx: CSF with listerial meningoencephalitis: misdiagnosis??
monocytes predominate. glucose level is often normal. low probability of observing Listeria in CSF (
74
Listeria tx
ampicillin + gentamycin. Alternative is TMP-SMX
75
Listeria prevention
NONE